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Results for "

amyloid b

" in MedChemExpress (MCE) Product Catalog:

41

Inhibitors & Agonists

3

Fluorescent Dyes

4

Peptides

2

Inhibitory Antibodies

13

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Products

2

Isotope-Labeled Compounds

3

Antibodies

1

Click Chemistry

2

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Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0044
    Ginsenoside Re
    4 Publications Verification

    Ginsenoside B2; Panaxoside Re; Sanchinoside Re

    		 Amyloid-β NF-κB JNK Endogenous Metabolite Neurological Disease Inflammation/Immunology Cancer
    Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
    Ginsenoside Re
  • HY-101855
    Emrusolmin

    Anle138b

    		 Amyloid-β Neurological Disease
    Emrusolmin (Anle138b), an oligomeric aggregation inhibitor, blocks the formation of pathological aggregates of prion protein (PrPSc) and of α-synuclein (α-syn). Emrusolmin strongly inhibits oligomer accumulation, neuronal degeneration, and disease progression in vivo. Emrusolmin has low toxicity and an excellent oral bioavailability and blood-brain-barrier penetration. Emrusolmin blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology .
    Emrusolmin
  • HY-103240
    Methoxy-X04
    5 Publications Verification

    		 Amyloid-β Others
    Methoxy-X04 is a fluorescent dye that crosses the blood-brain barrier and selectively binds to beta-pleated sheets found in dense core amyloid Aβ plaques. Methoxy-X04 retains in vitro binding affinity for amyloid b (Ab) fibrils (Ki= 26.8 nM). Methoxy-X04 is fluorescent and stains plaques, tangles, and cerebrovascular amyloid in postmortem sections of AD brain with good specificity .
    Methoxy-X04
  • HY-N0373
    Licochalcone B
    Maximum Cited Publications
    12 Publications Verification

    		 Amyloid-β Apoptosis NOD-like Receptor (NLR) Neurological Disease
    Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloid β (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
    Licochalcone B
  • HY-N2099
    Onjisaponin B
    2 Publications Verification

    Senegin III

    		 Autophagy Amyloid-β Caspase NF-κB Apoptosis Neurological Disease Metabolic Disease Inflammation/Immunology
    Onjisaponin B is an orally active natural product derived from Polygala tenuifolia. Onjisaponin B inhibits NF-κB p65. Onjisaponin B enhances autophagy and accelerates the degradation of mutant α-synuclein and huntingtin. Onjisaponin B reduces β-amyloid (Aβ) production. Onjisaponin B reduces radiation-induced cell apoptosis. Onjisaponin B has anti-oxidant and anti-inflammatory activities. Onjisaponin B can be used for neurological disease and radiation injury study, and its metabolite tenuifolin (TF) can enter the brain through the BBB .
    Onjisaponin B
  • HY-P2358
    PSMα3

    		NF-κB p38 MAPK Infection Inflammation/Immunology
    PSMα3 is an inhibitor of NF-κB p65 and p38 MAPK. PSMα3 forms membrane pores and binds to residues of human insulin B chain to inhibit insulin aggregation. PSMα3 forms α-type amyloid-like fibrils to exert cytotoxic effects, and acts as a functional amyloid virulence determinant of Staphylococcus aureus. PSMα3 is applicable to research related to spondyloarthritis, rheumatoid arthritis, insulin-derived amyloidosis, and Staphylococcus aureus infection .
    PSMα3
  • HY-N7046
    Silybin B

    Silibinin B

    		 Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B
  • HY-148089
    Eplontersen
    1 Publications Verification

    		 Transthyretin (TTR) Neurological Disease
    Eplontersen is a triantennary N-acetyl galactosamine (GalNAc3-7a)-conjugated antisense oligonucleotide targeting transthyretin (TTR) mRNA to inhibit production of both variant and wild-type TTR protein. Misfolded TTR induces amyloid fibrils formation in the heart and peripheral nerves, leads to amyloid TTR (ATTR) amyloidosis diseases .
    Eplontersen
  • HY-N1570
    Pterosin B

    		Salt-inducible Kinase (SIK) KLF Amyloid-β Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Pterosin B is an orally active indanone. Pterosin B can be obtained from Pteridium aquilinum. Pterosin B is a Sik3 signaling inhibitor. Pterosin B inhibits Klf5 expression and reduces β-amyloid deposition. Pterosin B prevents chondrocyte hypertrophy and osteoarthritis in mice. Pterosin B inhibits cardiomyocyte hypertrophy, improves cognitive impairment, and lowers blood glucose. Pterosin B can be used in research on arthritis, Alzheimer's disease, pathological cardiac hypertrophy and diabetes .
    Pterosin B
  • HY-P990301
    Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2)

    		Amyloid-β Neurological Disease
    Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2) is a mouse-derived IgG2b λ type antibody inhibitor, targeting to Amyloid-beta. Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2) recognizes unaggregated, oligomeric or fibrillar forms of Aβ42 and unaggregated Aβ40. Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2) is selective for human Aβ42 over Aβ40, but not amyloid precursor protein (APP). Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2) can immunostain human or rat and mouse tissue. Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2) can be used for detections of western blot, immunohistochemistry, immunofluorescence, immunoprecipitation and ELISA .
    Anti-Human/Mouse/Rat Amyloid-beta Antibody (MOAB-2)
  • HY-148089A
    Eplontersen sodium
    1 Publications Verification

    		 Transthyretin (TTR) Neurological Disease
    Eplontersen sodium the sodium salt form of Eplontersen (HY-148089). Eplontersen sodium is a triantennary N-acetyl galactosamine (GalNAc3-7a)-conjugated antisense oligonucleotide targeting transthyretin (TTR) mRNA to inhibit production of both variant and wild-type TTR protein. Misfolded TTR induces amyloid fibrils formation in the heart and peripheral nerves, leads to amyloid TTR (ATTR) amyloidosis diseases .
    Eplontersen sodium
  • HY-P991046
    Donanemab (Mouse IgG2b)

    		Amyloid-β Neurological Disease
    Donanemab (Mouse IgG2b) is a chimeric antibody composed of humanized variable regions and a mouse IgG2b backbone. Donanemab (Mouse IgG2b) is an anti-amyloid inhibitor used in Alzheimer's disease research.
    Donanemab (Mouse IgG2b)
  • HY-N1280
    Semilicoisoflavone B

    		Amyloid-β Neurological Disease
    Semilicoisoflavone B, an isoflavone, mainly derived from Glycyrrhiza uralensis Fisch.. Semilicoisoflavone B reduces amyloid β (Aβ) secretion by inhibiting β-secretase-1 (BACE1) expression and activity. Semilicoisoflavone B decreases BACE1 expression mainly through increasing PPARγ expression and inhibiting STAT3 phosphorylation .
    Semilicoisoflavone B
  • HY-N13742
    Dihydrohonokiol B

    Dihydrohonokiol

    		 GABA Receptor Neurological Disease
    Dihydrohonokiol B (Dihydrohonokiol) is an anxiolytic agent. Dihydrohonokiol B can reduce the neurotoxicity induced by amyloid β protein by stimulating the GABAC receptor. Dihydrohonokiol B can be used in the research of neurodegenerative diseases such as Alzheimer's disease .
    Dihydrohonokiol B
  • HY-W117986
    Aβ aggregation-IN-1

    		Amyloid-β Reactive Oxygen Species (ROS) Caspase Neurological Disease
    Aβ aggregation-IN-1 (Compound 1b) is a β-amyloid aggregation inhibitor/depolymerizer, with IC50 values of 3.92 μM and 7.19 μM, respectively. Aβ aggregation-IN-1 inhibits the activation of preformed β-amyloid fibrils, reactive oxygen species (ROS) and Caspase-3. Aβ aggregation-IN-1 can be used in research related to Alzheimer's disease .
    Aβ aggregation-IN-1
  • HY-DY1045
    Methoxy-X04 (solution)

    		Amyloid-β Neurological Disease
    Methoxy-X04 (solution) is a fluorescent dye that crosses the blood-brain barrier and selectively binds to beta-pleated sheets found in dense core amyloid Aβ plaques. Methoxy-X04 retains in vitro binding affinity for amyloid b (Ab) fibrils (Ki= 26.8 nM). Methoxy-X04 is fluorescent and stains plaques, tangles, and cerebrovascular amyloid in postmortem sections of AD brain with good specificity .
    Solvent and concentration: DMSO: 5 mg/mL
    Methoxy-X04 (solution)
  • HY-151962
    JNK3 inhibitor-5

    		JNK Apoptosis GSK-3 p38 MAPK Neurological Disease
    JNK3 inhibitor-5 (Compound 22b) is a potent and selective JNK3 inhibitor with an IC50 of 0.379 nM. JNK3 inhibitor-5 effectively protects the neuronal cells against amyloid beta-induced apoptosis. JNK3 inhibitor-5 has a high cell permeability and is predicted as BBB permeable .
    JNK3 inhibitor-5
  • HY-121817
    Sulfiram

    		Aldehyde Dehydrogenase (ALDH) Drug Intermediate Amyloid-β Infection Neurological Disease
    Sulfiram is a very weak aldehyde dehydrogenase (ALDH) inhibitor, with an IC50 value of 413 μM against Saccharomyces cerevisiae ALDH. As a photochemical precursor, Sulfiram undergoes photoconversion to form Disulfiram (HY-B0240), a potent ALDH inhibitor. Sulfiram inhibits the dimerization of the extracellular domain fragment (amino acid residues 230-624) of amyloid precursor protein (APP), alters the monomer-dimer equilibrium, induces conformational changes in the fragment, and enhances the production of sAPPα via α-cleavage of APP. Sulfiram can be used in research related to scabies and Alzheimer's disease .
    Sulfiram
  • HY-P11540
    CCKBR agonist-1

    		Cholecystokinin Receptor MMP Amyloid-β Neurological Disease
    CCKBR agonist-1 (Compound 3r1) is a Gq-protein-preferring cholecystokinin B receptor (CCKBR) agonist with an EC50 of 35 pM. CCKBR agonist-1 significantly increases the survival rate of neurons, with an EC50 of 37 pM. CCKBR agonist-1 can improve the cognitive decline in mice by upregulating α-secretase (ADAM10) and calcium signaling molecule PLCB4, reduce the number of amyloid β (Aβ) plaques, and promote long-term potentiation (LTP). CCKBR agonist-1 can be used for the study of Alzheimer's disease .
    CCKBR agonist-1
  • HY-N1570R
    Pterosin B (Standard)

    		Reference Standards Salt-inducible Kinase (SIK) KLF Amyloid-β Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Pterosin B (Standard) is the analytical standard of Pterosin B (HY-N1570). This product is intended for research and analytical applications. Pterosin B is an indanone. Pterosin B can be obtained from Pteridium aquilinum. Pterosin B is a Sik3 signaling inhibitor. Pterosin B inhibits Klf5 expression and reduces β-amyloid deposition. Pterosin B prevents chondrocyte hypertrophy and osteoarthritis in mice. Pterosin B inhibits cardiomyocyte hypertrophy, improves cognitive impairment, and lowers blood glucose. Pterosin B can be used in research on arthritis, Alzheimer's disease, pathological cardiac hypertrophy and diabetes .
    Pterosin B (Standard)
  • HY-N2099A
    (Z)-Onjisaponin B

    (Z)-Senegin III

    		 Drug Derivative Neurological Disease Metabolic Disease Inflammation/Immunology
    (Z)-Onjisaponin B ((Z)-Senegin III) is a derivative of Onjisaponin B (HY-N2099). Onjisaponin B is an orally active natural product derived from Polygala tenuifolia. Onjisaponin B inhibits NF-κB p65. Onjisaponin B enhances autophagy and accelerates the degradation of mutant α-synuclein and huntingtin. Onjisaponin B reduces β-amyloid (Aβ) production. Onjisaponin B reduces radiation-induced cell apoptosis. Onjisaponin B has anti-oxidant and anti-inflammatory activities. Onjisaponin B can be used for neurological disease and radiation injury study, and its metabolite tenuifolin (TF) can enter the brain through the BBB .
    (Z)-Onjisaponin B
  • HY-179167
    K2V-9

    		Cholinesterase (ChE) Monoamine Oxidase Neurological Disease
    K2V-9 is an AChE and MAO-B inhibitor with IC50 values of 1.72 μM and 0.950 μM against AChE and MAO-B, respectively. K2V-9 inhibits amyloid β self-aggregation and reduces ROS. K2V-9 has neuroprotective effects .
    K2V-9
  • HY-103383
    (R)-DRF053 dihydrochloride

    		CDK Casein Kinase Neurological Disease Cancer
    (R)-DRF053 dihydrochloride is a potent casein kinases 1 (CK1), CDK1/cyclin B and CDK5/p25 inhibitor with IC50s of 14 nM, 220 nM and 80 nM, respectively. (R)-DRF053 dihydrochloride prevents the CK1-dependent production of amyloid-beta in a cell model .
    (R)-DRF053 dihydrochloride
  • HY-P1854
    β-Amyloid (1-9)

    		Amyloid-β Neurological Disease
    β-Amyloid (1-9), an N-terminal fragment of beta amyloid, consists of amino acid residues 1 to 9. β-Amyloid (1-9) contains a B cell epitope, but it does not include T cell epitopes. Omission of residues 1 to 9 from the full-length Alzheimer'sβ-Amyloid peptide 1 to 40 does not prevent the peptide from forming amyloid fibrils or eliminate fibril polymorphism .
    β-Amyloid (1-9)
  • HY-146347
    MAO-B-IN-10

    		Monoamine Oxidase Amyloid-β Neurological Disease
    MAO-B-IN-10 (compound 4f) is a potent, selective, BBB-penetrated MAO-B (monoamine oxidase-B) inhibitor, with IC50 of 5.3 μM. MAO-B-IN-10 can inhibit (58.2%) and disaggregate (43.3%) self-mediated Aβ (amyloid β) aggregation. MAO-B-IN-10 can be use for Alzheimer’s disease research .
    MAO-B-IN-10
  • HY-152110
    AChE/MAO-IN-2

    		Cholinesterase (ChE) Monoamine Oxidase Neurological Disease
    Dual AChE-MAO B-IN-5, indanone derivative, is a potent dual AChE/MAO-B inhibitior with IC50 values of 0.0224, 0.0412, and 0.1116 μM for AChE, MAO-B and MAO-A, respectively. Dual AChE-MAO B-IN-5 has antioxidant activity and prevents β-amyloid plaque aggregation. Dual AChE-MAO B-IN-5 can be used for Alzheimer’s disease (AD) research .
    AChE/MAO-IN-2
  • HY-152114
    AChE/BChE/MAO-B-IN-4

    		Monoamine Oxidase Cholinesterase (ChE) Neurological Disease
    AChE/BChE/MAO-B-IN-4, an indan-1-one derivative, is a potent MAO-B inhibitor with an IC50 of 0.0393 μM for human MAO-B. AChE/BChE/MAO-B-IN-4 is a potent AChE and BChE enzyme inhibitor, with IC50s of 0.0458 μM and 0.075 μM for human AChE and BChE enzyme, respectively. AChE/BChE/MAO-B-IN-4 shows significant antioxidant activity and prevent β-amyloid plaque aggregation. AChE/BChE/MAO-B-IN-4 has the potential for Alzheimer's disease (AD) research .
    AChE/BChE/MAO-B-IN-4
  • HY-N0044R
    Ginsenoside Re (Standard)

    Ginsenoside B2(Standard); Panaxoside Re(Standard); Sanchinoside Re (Standard)

    		 Reference Standards Amyloid-β NF-κB JNK Endogenous Metabolite Neurological Disease Inflammation/Immunology Cancer
    Ginsenoside Re (Standard) is the analytical standard of Ginsenoside Re. This product is intended for research and analytical applications. Ginsenoside Re (Ginsenoside B2) is an extract from Panax notoginseng. Ginsenoside Re decreases the β-amyloid protein (Aβ). Ginsenoside Re plays a role in antiinflammation through inhibition of JNK and NF-κB.
    Ginsenoside Re (Standard)
  • HY-P2358A
    PSMα3 TFA

    		NF-κB p38 MAPK Infection Inflammation/Immunology
    PSMα3 TFA is an inhibitor of NF-κB p65 and p38 MAPK. PSMα3 TFA forms membrane pores and binds to residues of human insulin B chain to inhibit insulin aggregation. PSMα3 TFA forms α-type amyloid-like fibrils to exert cytotoxic effects, and acts as a functional amyloid virulence determinant of Staphylococcus aureus. PSMα3 TFA is applicable to research related to spondyloarthritis, rheumatoid arthritis, insulin-derived amyloidosis, and Staphylococcus aureus infection .
    PSMα3 TFA
  • HY-N0373R
    Licochalcone B (Standard)

    		Reference Standards Amyloid-β Apoptosis NOD-like Receptor (NLR) Neurological Disease
    Licochalcone B (Standard) is the analytical standard of Licochalcone B. This product is intended for research and analytical applications. Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloid β (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
    Licochalcone B (Standard)
  • HY-N7046S
    Silybin B-d3

    Silibinin B-d3

    		 Isotope-Labeled Compounds Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B-d3 (Silibinin B-d3) is a deuterated Silybin B (HY-N7046). Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B-d3
  • HY-N7046R
    Silybin B (Standard)

    Silibinin B (Standard)

    		 Reference Standards JNK Amyloid-β p38 MAPK Apoptosis Neurological Disease Cancer
    Silybin (Silibinin B) (Standard) is the analytical standard of Silybin B (HY-N7046). This product is intended for research and analytical applications. Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B (Standard)
  • HY-163746
    BuChE-IN-11

    		Cholinesterase (ChE) Neurological Disease
    BuChE-IN-11 (Compound 3b-1) is an selective BuChE inhibitor with an IC50 of 0.44 μM for hBuChE. BuChE-IN-11 has high blood-brain barrier permeability and exhibits strong antioxidant activity due to its free radical scavenging properties. BuChE-IN-11 interacts with the choline binding site, acetyl binding site, and peripheral anionic site, exhibiting submicromolar BuChE inhibitory activity and preventing β-amyloid (Aβ) self-aggregation. BuChE-IN-11 holds promise for research in the field of Alzheimer's disease .
    BuChE-IN-11
  • HY-B1794S
    Thiethylperazine-d3

    		Isotope-Labeled Compounds Dopamine Receptor Histamine Receptor Bacterial Amyloid-β Infection Neurological Disease
    Thiethylperazine-d3 is the deuterium labeled Thiethylperazinee (HY-B1794). Thiethylperazine, a phenothiazine derivate, is an orally active and potent dopamine D2-receptor and histamine H1-receptor antagonist. Thiethylperazine is also a selective ABCC1activator that reduces amyloid-β (Aβ) load in mice. Thiethylperazine has anti-emetic, antipsychotic and antimicrobial effects .
    Thiethylperazine-d3
  • HY-149211
    AChE/BChE-IN-12

    		Cholinesterase (ChE) Beta-secretase Amyloid-β Neurological Disease
    AChE/BChE-IN-12 (compound 10b), a 3,5-dimethoxy analogue, is a potent AChE, BChE, and β-secretase-1 (BACE-1) inhibitor, with IC50 values of 2.57, 3.26, and 10.65 μM, respectively. AChE/BChE-IN-12 crosses the blood-brain barrier via passive diffusion and inhibits the self-aggregation of amyloid-β monomers. AChE/BChE-IN-12 can be used for Alzheimer’s disease (AD) research .
    AChE/BChE-IN-12
  • HY-155085
    hAChE-IN-3

    		Monoamine Oxidase Amyloid-β Cholinesterase (ChE) Neurological Disease
    hAChE-IN-3 (compounds 5c) is a potent and blood-brain barrier permeable AChE, BuChE， MAO-B-IN-1 and BACE-1 inhibitor, with IC50 values of 0.44, 0.08, 5.15 and 0.38 μM, respectively. hAChE-IN-3 has antioxidant activity and metal chelating ability. In addition, hAChE-IN-3 can bind to peripheral anion sites, and affect β amyloid and reduce Alzheimer's-associated neurodegeneration. hAChE-IN-3 has the potential for the research of Alzheimer's disease .
    hAChE-IN-3
  • HY-158978
    Multitarget AD inhibitor-2

    		Cholinesterase (ChE) Monoamine Oxidase Neurological Disease
    Multitarget AD inhibitor-2 (Compound VN-19) is a multitargeting inhibitor acetylcholinesterase (AChE, IC50=0.14 μM), butyrylcholinesterase (BChE, IC50=11.6 μM), monoamine oxidase B (MAO B, IC50=0.45 μM). Multitarget AD inhibitor-2 inhibits self-induced aggregation of amyloid beta protein Aβ1-42 (inhibition rate is 47.3% at 20 μM), and downregulates the level of ROS in SH-SY5Y (80 inhibition rate at 25 μM). Multitarget AD inhibitor-2 ameliorates the cognitive decline in Scopolamine (HY-N0296)-induced Alzheimer’s Disease zebrafish models .
    Multitarget AD inhibitor-2
  • HY-103240R
    Methoxy-X04 (Standard)

    		Reference Standards Amyloid-β Others
    Methoxy-X04 (Standard) is the analytical standard of Methoxy-X04 (HY-103240). This product is intended for research and analytical applications. Methoxy-X04 is a fluorescent dye that crosses the blood-brain barrier and selectively binds to beta-pleated sheets found in dense core amyloid Aβ plaques. Methoxy-X04 retains in vitro binding affinity for amyloid b (Ab) fibrils (Ki= 26.8 nM). Methoxy-X04 is fluorescent and stains plaques, tangles, and cerebrovascular amyloid in postmortem sections of AD brain with good specificity .
    Methoxy-X04 (Standard)
  • HY-182786
    MAO-B-IN-56

    		Cholinesterase (ChE) Monoamine Oxidase Beta-secretase COX Amyloid-β Neurological Disease
    MAO-B-IN-56 is a multi-target-directed ligand with AChE, BChE, MAO-B, and BACE1 inhibitory activity, with IC50 values of 0.35 μM, 3.22 μM, 0.14 μM, and 3.85 μM respectively, and shows selectivity for AChE over BChE and MAO-B over MAO-A.MAO-B-IN-56 reduces amyloid-beta production, reduces paw edema, improves spatial memory, and enhances Alzheimer's disease hallmarks and associated histopathological alterations.MAO-B-IN-56 can be used for the research of alzheimer's disease .
    MAO-B-IN-56
  • HY-175523
    MAO-B-IN-48

    		Monoamine Oxidase Cholinesterase (ChE) Amyloid-β Neurological Disease
    MAO-B-IN-48 is a selective MAO-B inhibitor (IC50 = 0.09 μM, Ki = 0.02 μM). MAO-B-IN-48 exhibits inhibitory activity against hBChE (IC50 = 1.10 μM, Ki = 0.43 μM) and AChE (IC50 = 0.56 μM, Ki = 0.14 μM). MAO-B-IN-48 suppresses self-induced aggregation of toxic β-amyloid peptides and exerts antioxidant activity, including DPPH radical scavenging, CUPRAC copper ion reduction, and superoxide anion scavenging. MAO-B-IN-48 can be used for the study of Alzheimer's disease (AD) .
    MAO-B-IN-48
  • HY-101855R
    Emrusolmin (Standard)

    Anle138b (Standard)

    		 Reference Standards Amyloid-β Neurological Disease
    Emrusolmin (Standard) (Anle138b (Standard)) is the analytical standard of Emrusolmin (HY-101855). This product is intended for research and analytical applications. Emrusolmin (Anle138b), an oligomeric aggregation inhibitor, blocks the formation of pathological aggregates of prion protein (PrPSc) and of α-synuclein (α-syn). Emrusolmin strongly inhibits oligomer accumulation, neuronal degeneration, and disease progression in vivo. Emrusolmin has low toxicity and an excellent oral bioavailability and blood-brain-barrier penetration. Emrusolmin blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology .
    Emrusolmin (Standard)

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